ArticleBasic research in cardiology2024
Circular RNA circZFPM2 regulates cardiomyocyte hypertrophy and survival.
Article in Basic research in cardiology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.
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Who cites it
17 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Noncoding RNA as potential therapeutics to rescue mitochondrial dysfunction in cardiovascular diseases.American journal of physiology. Heart and circulatory physiology · 2025Pooled it
- Myofilament-level effects of aficamten increase diastolic chamber volumes and maintain cardiac output through preserved length-dependent force generation in healthy rat and canine myocardium.Basic research in cardiology · 2026Article
- RNA splicing and cardiovascular disease: a guide for cardiologists.European heart journal · 2026Review
- Circular RNAs: Unlocking new avenues in cardiometabolic disease management.The Journal of physiology · 2026Review
- Circular RNAs in Cardiovascular Diseases: From Regulatory Networks to Functional Effectors.International journal of molecular sciences · 2026Review
- FTO-Eci1 Axis Mediates Exercise-Induced Cardioprotection in Pressure Overload Mice.Biomolecules · 2026Article
- The silent dialogue between cells: regulatory roles of non-coding RNAs in cardiovascular disease.Frontiers in cell and developmental biology · 2026Review
- Circular RNA: From non-coding regulators to functional protein encoders.Pharmaceutical science advances · 2025Review
- Overview of exosomal non-coding RNAs in cardiovascular disease using high throughput sequencing.European journal of pharmacology · 2025Review
- A circular RNA derived from the ryanodine receptor 2 locus controls cardiac hypertrophy and calcium handling.Cellular and molecular life sciences : CMLS · 2025Article
- Circular RNA circFTO promotes pressure overload-induced cardiac hypertrophy by encoding a novel protein FTO-36aa.Journal of thoracic disease · 2025Article
- Circular RNA circIGF1R controls cardiac fibroblast proliferation through regulation of carbohydrate metabolism.Scientific reports · 2025Article
- QRICH1 regulates ATF6 transcription to affect pathological cardiac hypertrophy progression.Molecular medicine (Cambridge, Mass.) · 2025Article
- Emerging role and clinical applications of circular RNAs in human diseases.Functional & integrative genomics · 2025Review
- Stem-Cell Derived Exosomal microRNAs as Biomarkers and Therapeutics for Pediatric Cardiovascular Disease.Current treatment options in cardiovascular medicine · 2025Review
- Circular RNAs in Cardiovascular Diseases: Molecular Mechanisms, Therapeutic Advances, and Innovations.Genes · 2024Review
- Review
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Authors and funding
25 authors.
Funding
Abstract
Hypertrophic cardiomyopathy (HCM) constitutes the most common genetic cardiac disorder. However, current pharmacotherapeutics are mainly symptomatic and only partially address underlying molecular mechanisms. Circular RNAs (circRNAs) are a recently discovered class of non-coding RNAs and emerged as specific and powerful regulators of cellular functions. By performing global circRNA-specific next generation sequencing in cardiac tissue of patients with hypertrophic cardiomyopathy compared to healthy donors, we identified circZFPM2 (hsa_circ_0003380). CircZFPM2, which derives from the ZFPM2 gene locus, is a highly conserved regulatory circRNA that is strongly induced in HCM tissue. In vitro loss-of-function experiments were performed in neonatal rat cardiomyocytes, human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs), and HCM-patient-derived hiPSC-CMs. A knockdown of circZFPM2 was found to induce cardiomyocyte hypertrophy and compromise mitochondrial respiration, leading to an increased production of reactive oxygen species and apoptosis. In contrast, delivery of recombinant circZFPM2, packaged in lipid-nanoparticles or using AAV-based overexpression, rescued cardiomyocyte hypertrophic gene expression and promoted cell survival. Additionally, HCM-derived cardiac organoids exhibited improved contractility upon CM-specific overexpression of circZFPM2. Multi-Omics analysis further promoted our hypothesis, showing beneficial effects of circZFPM2 on cardiac contractility and mitochondrial function. Collectively, our data highlight that circZFPM2 serves as a promising target for the treatment of cardiac hypertrophy including HCM.
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